PROJECT SUMMARY Although late sleep timing is emerging as a significant risk factor for chronic health conditions, a gap exists in understanding the mechanisms underlying the development of a delayed sleep phenotype. This is particularly true for early childhood, a sensitive period in the maturation of sleep regulation and a time when poor sleep patterns first emerge. Late sleep timing and behavioral sleep problems are prevalent in ~25% of preschoolers. Central to the proposed research are our published data indicating that evening sleep problems and delayed sleep timing are linked to a later timing of the circadian system. Light is the primary zeitgeber of the circadian clock, and even low intensities of light can suppress melatonin levels and delay or advance circadian timing. For several reasons, we believe that light may be significant for determining sleep and circadian timing in early childhood: (1) the melatonin suppressing effects of evening light in school-age children are ~2x that of adults; (2) children are proposed to be more sensitive to light than adults based upon differences in ophthalmological features; (3) the enhanced transmission rate of the crystal lens in developing humans is prominent in the short wavelength of light, which is emitted from light-emitting diode electronic devices; and (4) media use has almost tripled in preschoolers in the past years and is associated with delayed sleep timing and evening sleep problems. This research will build upon our pilot data showing that 1 h of bright light before bedtime leads to high (~90%) suppression of melatonin in preschoolers. We will examine the sensitivity of the circadian clock to varying intensities of morning and evening light in preschool age children. We will obtain key data on light as a pathway by which delayed sleep timing is promoted and early sleep timing is protected in early childhood. Children (ages 3.0-4.9 years) follow a stable sleep schedule (7 days) and then enter an in-home dim-light environment (3 days), where they are exposed to a single illuminance of light for 3 h, ranging from 1 lux to 10,000 lux in either the morning (Advance condition; n=45) or the evening (Delay condition; n=45) starting 1.5 h before scheduled bedtime or wake time. Salivary melatonin onset assessments are performed using our established protocol at Baseline and the day following light exposure. In Aim 1, we will examine the sensitivity of the circadian clock to evening light, and in Aim 2, we will examine the sensitivity of the circadian clock to morning light. We hypothesize that evening/morning light exposure will induce circadian phase shifts and acute melatonin suppression in a non-linear intensity-dependent manner. This research is innovative, timely, and we expect that results will have a high payoff by addressing fundamental knowledge gaps relevant to modifiable targets (i.e., light, circadian timing) that may promote risk for or resilience to late sleep timing. Our data will make important contributions to the field by establishing the minimum and saturating light levels needed to produce circadian phase shifts, which are critical for making recommendations about light exposure and developing countermeasures for late sleep timing in early childhood.